Heart wall tension reduction apparatus and method

ABSTRACT

Devices and methods for treatment of a failing heart by reducing the heart wall stress. The device can be one which reduces wall stress throughout the cardiac cycle or only a portion of the cardiac cycle.

RELATED APPLICATIONS

This application is a continuation-in-part of U.S. application Ser. No.09/985,361 of Cyril J. SCHWEICH, Jr. et al. for HEART WALL TENSIONREDUCTION APPARATUS AND METHOD, filed Nov. 2, 2001 now U.S. Pat. No.6,589,160, which is a continuation of U.S. application Ser. No.09/697,597, filed Oct. 27, 2000, now U.S. Pat. No. 6,332,864, which is acontinuation of application Ser. No. 09/492,777, filed Jan. 28, 2000,now U.S. Pat. No. 6,162,168, which is a continuation of application Ser.No. 08/778,277, filed Jan. 2, 1997, now U.S. Pat. No. 6,050,936.

This application also is a continuation-in-part of U.S. application Ser.No. 09/843,078 of Todd J. MORTIER et al. for STRESS REDUCTION APPARATUSAND METHOD, filed Apr. 27, 2001 now U.S. Pat. No. 6,402,680, which is acontinuation of application Ser. No. 09/522,068, filed Mar. 9, 2000, nowU.S. Pat. No. 6,264,602, which is a continuation of application Ser. No.09/124,321, filed Jul. 29, 1998, now U.S. Pat. No. 6,077,214.

FIELD OF THE INVENTION

The present invention pertains to the field of apparatus for treatmentof a failing heart. In particular, the apparatus of the presentinvention is directed toward reducing the wall stress in the failingheart.

BACKGROUND OF THE INVENTION

The syndrome of heart failure is a common course for the progression ofmany forms of heart disease. Heart failure may be considered to be thecondition in which an abnormality of cardiac function is responsible forthe inability of the heart to pump blood at a rate commensurate with therequirements of the metabolizing tissues, or can do so only at anabnormally elevated filling pressure. There are many specific diseaseprocesses that can lead to heart failure with a resulting difference inpathophysiology of the failing heart, such as the dilatation of the leftventricular chamber. Etiologies that can lead to this form of failureinclude idiopathic cardiomyopathy, viral cardiomyopathy, and ischemiccardiomyopathy.

The process of ventricular dilatation is generally the result of chronicvolume overload or specific damage to the myocardium. In a normal heartthat is exposed to long term increased cardiac output requirements, forexample, that of an athlete, there is an adaptive process of slightventricular dilation and muscle myocyte hypertrophy. In this way, theheart fully compensates for the increased cardiac output requirements.With damage to the myocardium or chronic volume overload, however, thereare increased requirements put on the contracting myocardium to such alevel that this compensated state is never achieved and the heartcontinues to dilate.

The basic problem with a large dilated left ventricle is that there is asignificant increase in wall tension and/or stress both during diastolicfilling and during systolic contraction. In a normal heart, theadaptation of muscle hypertrophy (thickening) and ventricular dilatationmaintain a fairly constant wall tension for systolic contraction.However, in a failing heart, the ongoing dilatation is greater than thehypertrophy and the result is a rising wall tension requirement forsystolic contraction. This is felt to be an ongoing insult to the musclemyocyte resulting in further muscle damage. The increase in wall stressis also true for diastolic filling. Additionally, because of the lack ofcardiac output, there is generally a rise in ventricular fillingpressure from several physiologic mechanisms. Moreover, in diastolethere is both a diameter increase and a pressure increase over normal,both contributing to higher wall stress levels. The increase indiastolic wall stress is felt to be the primary contributor to ongoingdilatation of the chamber.

Prior art treatments for heart failure fall into three generallycategories. The first being pharmacological, for example, diuretics. Thesecond being assist systems, for example, pumps. Finally, surgicaltreatments have been experimented with, which are described in moredetail below.

With respect to pharmacological treatments, diuretics have been used toreduce the workload of the heart by reducing blood volume and preload.Clinically, preload is defined in several ways including leftventricular end diastolic pressure (LVEDP), or left ventricular enddiastolic volume (LVEDV). Physiologically, the preferred definition isthe length of stretch of the sarcomere at end diastole. Diuretics reduceextra cellular fluid which builds in congestive heart failure patientsincreasing preload conditions. Nitrates, arteriolar vasodilators,angiotensin converting enzyme inhibitors have been used to treat heartfailure through the reduction of cardiac workload through the reductionof afterload. Afterload may be defined as the tension or stress requiredin the wall of the ventricle during ejection. Inotropes like digoxin arecardiac glycosides and function to increase cardiac output by increasingthe force and speed of cardiac muscle contraction. These drug therapiesoffer some beneficial effects but do not stop the progression of thedisease.

Assist devices include mechanical pumps and electrical stimulators.Mechanical pumps reduce the load on the heart by performing all or partof the pumping function normally done by the heart. Currently,mechanical pumps are used to sustain the patient while a donor heart fortransplantation becomes available for the patient. Electricalstimulation such as bi-ventricular pacing have been investigated for thetreatment of patients with dilated cardiomyopathy.

There are at least three surgical procedures for treatment of heartfailure: 1) heart transplant; 2) dynamic cardiomyoplasty; and 3) theBatista partial left ventriculectomy. Heart transplantation has seriouslimitations including restricted availability of organs and adverseeffects of immunosuppressive therapies required following hearttransplantation. Cardiomyoplasty includes wrapping the heart withskeletal muscle and electrically stimulating the muscle to contractsynchronously with the heart in order to help the pumping function ofthe heart. The Batista partial left ventriculectomy includes surgicallyremodeling the left ventricle by removing a segment of the muscularwall. This procedure reduces the diameter of the dilated heart, which inturn reduces the loading of the heart. However, this extremely invasiveprocedure reduces muscle mass of the heart.

SUMMARY OF THE INVENTION

The present invention pertains to a non-pharmacological, passiveapparatus for the treatment of a failing heart. The device is configuredto reduce the tension in the heart wall. It is believed to reverse, stopor slow the disease process of a failing heart as it reduces the energyconsumption of the failing heart, decrease in isovolumetric contraction,increases sarcomere shortening during contraction and an increase inisotonic shortening in turn increases stroke volume. In embodiments, thedevice reduces wall tension during diastole (preload) and systole.

In an embodiment, the apparatus includes a compression member fordrawing at least two walls of a heart chamber toward each other toreduce the radius or area of the heart chamber in at least one crosssectional plane. In one embodiment of the apparatus, a frame is providedfor supporting the compression member.

Yet another embodiment of the invention includes a clamp having two endsbiased toward one another for drawing at least two walls of a heartchamber toward each other. The clamp includes at least two ends havingatraumatic anchoring member disposed thereon for engagement with theheart or chamber wall.

The present invention also pertains to a device and method for reducingmechanical heart wall muscle stress. Heart muscle stress is a stimulusfor the initiation and progressive enlargement of the left ventricle inheart failure. Reduction of heart wall stress with the devices andmethods disclosed herein is anticipated to substantially slow, stop orreverse the heart failure disease process. Although the primary focus ofthe discussion of the devices and methods of the present inventionherein relates to heart failure and the left ventricle, these devicesand method could be used to reduce stress in the heart's other chambers.

The devices and methods of the present invention can reduce heart wallstress throughout the cardiac cycle including end diastole and endsystole. Alternatively, they can be used to reduce wall stress duringthe portions of the cardiac cycle not including end systole. Thosedevices which operate throughout the cardiac cycle are referred toherein as “full cycle splints”. Those devices which do not operate toreduce wall stress during end stage systole are referred to as“restrictive devices”. Restrictive devices include both “restrictivesplints” which alter the geometric shape of the left ventricle, and“wraps” which merely limit the magnitude of the expansion of the leftventricle during diastolic filling without a substantial shape change.

While it is desirable to reduce wall stress for the treatment of heartfailure, to slow or reverse the disease process and to increase heartwall muscle shortening and pumping efficiency, it is also desirable tomaintain or improve stroke volume and allow for variable preload.

Improving muscle shortening both total length change and extent at endsystole, is particularly important in symptomatic heart failure whereinthe heart has decreased left ventricle function and has enlarged. Fullcycle splinting can be used to obtain a substantial increase in muscleshortening. Improved shortening will lead to an increase in pumpfunction, and chronically may result in muscle strengthening andreversal of the disease because of increased pumping efficiency. Theincrease in shortening should be balanced against a reduction in chambervolume.

In asymptomatic, early stage heart failure, it may be possible to useonly a restrictive device or method as elevated wall stress isconsidered to be an initiator of muscle damage and chamber enlargement.Restrictive devices and methods acting during diastole will reduce themaximum wall stress experienced during end diastole and early systole.It should be understood that restrictive devices and methods can be usedin combination with full cycle splinting to more precisely control ormanipulate stress reduction throughout the cardiac cycle.

BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1 is a vertical side view of a heart including a transventricularsplint and band splint;

FIG. 2 is a horizontal cross section of the heart, splint and bandsplint of FIG. 1;

FIG. 3 is a graph showing the relationship between stress and strain forthe sarcomeres of the left ventricle for a normal and failing heartthroughout the cardiac cycle;

FIG. 4 is an idealized horizontal cross section of a left ventriclesplinted to form two lobes;

FIG. 5 is an idealized horizontal cross sectional left ventriclesplinted to form three lobes;

FIG. 6 is a vertical view of a heart including two transventricularsplints and two band splints;

FIG. 7 is a cross sectional view of the heart, a band splint and asplint of FIG. 6;

FIG. 8 is a vertical view of a heart including a transventricular splintand a partial band splint;

FIG. 9 is a horizontal cross sectional view of the heart, splint andband splint of FIG. 8;

FIG. 10 is a horizontal cross section of a heart including a splinthaving full cycle and restrictive elements at the beginning of diastolicfilling;

FIG. 11 is a view of the splint of FIG. 10 at end diastole;

FIG. 12 is a vertical view of the heart in phantom line including a bandsplint;

FIG. 13 is an alternate embodiment of the band splint of FIG. 12;

FIG. 14 is an alternate embodiment of the band splint of FIG. 12;

FIG. 15 is an alternate embodiment of the band splint of FIG. 12;

FIG. 16 is a vertical view of a heart including a partialcircumferential strap;

FIG. 17 is a horizontal cross sectional view of the heart and strap ofFIG. 16;

FIG. 18 is a vertical view of a heart in phantom line including a singleelement wrap including longitudinal axis securing points;

FIG. 19 is an alternate embodiment of the wrap of FIG. 18;

FIG. 20 is an alternate embodiment of the wrap of FIG. 18;

FIG. 21 is an alternate embodiment of the wrap of FIG. 18;

FIG. 22 is a vertical view of the heart including a mesh wrap;

FIG. 23 is a cross sectional view of a patient's torso and heart showinga band splint anchored to the patient's ribs;

FIG. 24 is a partial vertical view of the heart and band splint of FIG.23;

FIG. 25 is a partial vertical view of a failing heart;

FIG. 26 is a cross sectional view of the heart of FIG. 25;

FIG. 27 is a vertical view of the heart for decreasing the horizontalradius of the ventricles and increasing their vertical length;

FIG. 28 is an exaggerated vertical view of the heart of FIG. 25elongated by the device of FIG. 27;

FIG. 29 is a view of the cross section of FIG. 26 showing the decreasein radius of the ventricles;

FIG. 30 is a horizontal cross sectional view of the left and rightventricles including reinforcement loops;

FIG. 31 is an alternate embodiment of the reinforcing loops of FIG. 30;

FIG. 32 shows a vertical view of the heart including the reinforcementloops of FIG. 31 and a rigid shape changing member;

FIG. 33 is a transverse cross-section of the left and right ventriclesof a human heart showing the placement of an external compression framestructure in accordance with the present invention;

FIG. 34 is a transverse cross-section of the left and right ventriclesof a human heart showing a clamp in accordance with the presentinvention;

FIG. 35 is a idealized cylindrical model of a left ventricle of a humanheart;

FIG. 36 is a splinted model of the left ventricle of FIG. 35;

FIG. 37 is a transverse cross-sectional view of FIG. 36 showing variousmodeling parameters;

FIG. 38 is a transverse cross-section of the splinted left ventricle ofFIG. 36 showing a hypothetical force distribution; and

FIG. 39 is a second transverse cross-sectional view of the model leftventricle of FIG. 36 showing a hypothetical force distribution.

DESCRIPTION OF THE EMBODIMENTS

The present invention is directed at reducing wall stress in a failingheart. Diastolic wall stress is considered to be an initiator of muscledamage and chamber enlargement. For this reason, it is desirable toreduce diastolic wall stress to prevent the progression of the disease.The significant impact of stress occurs at all stages and functionallevels of heart failure, however, independent of the original causes.For example, in asymptomatic early stages of heart failure, mechanicalstress can lead to symptomatic heart failure marked by an enlarged heartwith decreased left ventricle function. As the heart enlarges,mechanical stress on the heart wall increases proportionally to theincreasing radius of the heart in accordance with LaPlace's Law. It canthus be appreciated that as stress increases in symptomatic heartfailure, those factors that contributed to increasing stress alsoincrease. Thus, the progression of the disease accelerates to late stageheart failure, end stage heart failure and death unless the disease istreated.

Three parameters influence mechanical stress on the muscle. These are:(1) muscle mass, i.e., as reflected by the thickness of the muscle; (2)pressure in the chamber which is a function of the resistance to bloodflow of the patient's vasculature and the volume of blood within thepatient; and (3) chamber geometry. The present invention pertains todevices and methods for directly and passively changing chamber geometryto lower wall stress. In addition to treatment of heart failure, thedevices and methods of the present invention also lend themselves toapplication in the case of a decrease in cardiac function caused by, forexample, acute myocardial infarction.

The devices disclosed herein for changing chamber geometry are referredto as “splints”. In addition to splints, wraps which can be placedaround the heart can limit muscle stress without the chamber shapechange. When a wrap is used, wall stress is merely transferred to thewrap, while the generally globular shape of the heart is maintained. Awrap could be used in conjunction with a splint to modulate heart wallstress reduction at various stages of the cardiac cycle.

The present invention includes a number of splint embodiments. Splintsand wraps can be classified by where in the cardiac cycle they engagethe heart wall, i.e., mechanically limit the size of the left ventriclein the case of wraps and change the geometry of the ventricle in thecase of splints. If a splint or wrap only begins to engage duringdiastolic filling, the splint can be termed a “restrictive splint”. Ifthe splint or wrap is engaged throughout the cardiac cycle, both duringdiastolic filling and systolic contraction and ejection, the splint canbe termed a “full cycle splint”. The wrap will generally be arestrictive device which begins to engage during diastolic filling toincrease the elastance (reduces compliance) of the chamber. If a wrap ismade from elastic material it may engage full cycle, but the forcerequired to elongate the wrap will increase as diastolic fillingprogresses, preload strain will be reduced without an improvement insystolic contraction.

FIG. 1 is a view of a heart A in a normal, generally verticalorientation. A wrap 11 surrounds heart A and a transventricular splint12 extends through the heart and includes an anchor or anchor pad 13disposed on opposite sides of the heart. FIG. 2 is a horizontal crosssectional view of heart A taken through wrap 11 and splint 12. Splint 12includes a tension member 15 extending through left ventricle B. Anchorpads 13 are disposed at each end of tension member 15. Right ventricle Cis to the left of left ventricle B.

In FIG. 1, wrap 11 and splint 12 are shown engaged with heart A. In FIG.2, heart A is shown spaced from wrap 11 except at anchor pads 13. InFIG. 2, heart A is thus at a point in the cardiac cycle where themuscles are shortening during systole, or have yet to stretchsufficiently during diastolic expansion to reach wrap 11. Accordingly,wrap 11 can be considered a restrictive device as it does not engage theheart full cycle. Although wrap 11 is in contact with heart A at pads13, only the splint is providing a compressive force to change the shapeof the heart and limiting the stress of the heart in FIG. 2.

If heart A, as shown in FIG. 2 is at end systole, transventricularsplint 12 is a full cycle device as the cross section of left ventricleB does not have the generally circular unsplinted shape. Alternately,wrap 11 could be secured to heart A by sutures or other means thansplint 12, in which case wrap 11 would be merely a restrictive device.It should be noted that unless wrap 11 extends vertically along heart Aa sufficient amount, as heart A expands and engages wrap 11, the portionof left ventricle B disposed above or below wrap 11 could expandsubstantially further than that portion of the left ventricle wallrestrained by wrap 11. In such a case, left ventricle B could have abi-lobed shape in a vertical cross section. As such, the wrap 11 wouldnot be merely limiting the size of the left ventricle, but ratherinducing a shape change in the left ventricle. In such a case, theelement 11 would not be a wrap, but rather a splint which could bereferred to as a “band splint”.

Each of the splints, wraps and other devices disclosed in thisapplication preferably do not substantially deform during the cardiaccycle such that the magnitude of the resistance to the expansion orcontraction of the heart provided by these devices is reduced bysubstantial deflection. It is, however, contemplated that devices whichdeflect or elongate elastically under load are within the scope of thepresent invention, though not preferred. The materials from which eachdevice are formed must be biocompatible and are preferably configured tobe substantially atraumatic.

The distinction between restrictive devices, such as restrictive splintsand wraps, and full cycle splints and wraps, can be better understood byreference to FIG. 3. FIG. 3 is a plot of sarcomere, i.e., heart wallmuscle, stress in (g/cm²) versus strain throughout a normal cardiaccycle N, and a failing heart cardiac cycle F. The cardiac cycles orloops shown on FIG. 3 are bounded by the normal contractility curveN_(c) and failing heart contractility curve F_(c) above and to the left,and the diastolic filling curve 12 toward the bottom and right.Contractility is a measure of muscle stress at an attainable systolicstress at a given elongation or strain. It can be appreciated that themuscle contractility N_(c) of normal muscle tissue is greater than thecontractility F_(c) of the muscle tissue of a failing heart. Thediastolic filling curve 12 is a plot of the stress in the muscle tissueat a given elongation or strain when the muscle is at rest.

An arbitrary beginning of the normal cardiac cycle N can be chosen atend diastole 14, where the left ventricle is full, the aortic valve isclosed. Just after end diastole 14, systole begins, the sarcomeremuscles become active and the mitral valve closes, increasing musclestress without substantially shortening (sometimes referred to as“isovolumic contraction”). Stress increases until the aortic valve opensat 16. Isotonic shortening begins and stress decreases and the musclesshorten until end systole 18, where the blood has been ejected from theleft ventricle and the aortic valve closes. After end systole 18,diastole begins, the muscles relax without elongating until diastolicfilling begins when the mitral valve opens at 20. The muscles thenelongate while the mitral valve remains open during diastolic fillinguntil end diastole 14. The total muscle shortening and lengtheningduring the normal cycle N is N_(S).

An analogous cycle F also occurs in a failing heart. As the leftventricle has dilated, in accordance with LaPlace's Law, the largerradius of a dilated left ventricle causes stress to increase at a givenblood pressure. Consequently, a failing heart must compensate tomaintain the blood pressure. The compensation for the increased stressis reflected in the shift to the right of failing heart cardiac cycle Frelative to the normal cycle N. The stress at end diastole 22 iselevated over the stress at end diastole 14 of the normal heart. Asimilar increase can be seen for the point at which the aortic valveopens 24, end systole 26 and the beginning of diastolic filling 28relative to the analogous points for the normal cycle N. Muscleshortening and elongation F_(S) throughout the cycle is also reduced inview of the relative steepening of the diastolic curve 12 to the rightand the flatter contractility curve F_(c) relative to the normalcontractility N_(c).

By reference to the heart cycle stress strain graph of FIG. 3, theeffect on mechanical muscle stress and strain caused by the use of thedevices and methods of the present invention can be illustrated.Restrictive devices begin to engage during diastolic filling, which inthe case of a failing heart occurs along diastolic filling curve 12between point 28 and 22. Restrictive devices do not engage at endsystole 26. Thus, the acute effect of placement of a restrictive deviceis to reduce muscle stress at end diastole relative to the stress atpoint 22, and shift the line 22-24 to the left reducing muscleshortening and elongation F_(S). Acutely, the cardiac cycle will stilloperate between the failing heart contractility curve F_(c) and thediastolic filling curve 12. If chronic muscle contractility increasessuch that the muscle contractility curve F_(c) shifts back toward thenormal heart contractility curve N_(C) as a consequence of the stressreduction, the stress/strain curve F of the cardiac cycle will shift tothe left reducing mechanical stress still further.

The effect on the stress/strain relationship of a full cycle splint willacutely shift the entire stress/strain curve F for the cycle to theleft. That is, stress is reduced at both end diastole 22 and end systole26. Muscle shortening and elongation F_(s) will increase acutely. If, asin the case of a restrictive splint, muscle contractility F_(C)improves, the entire cardiac cycle curve F will shift further to theleft reducing mechanical stress still further.

The type and magnitude of shape change are important factors indetermining the effectiveness of splinting. There are several types oflower stress cardiac geometries that can be created from an enlargedglobular left ventricular chamber typically associate with heartfailure. They include lobed, disc-like, narrowed elongate, and multiplevertically stacked bulbs.

FIG. 4 shows an idealized horizontal cross section of a left ventricle30 subdivided into two symmetrical lobes 32 and 34 having an arc passingthrough an angle θ>π, and a radius R. Lobes 32 and 34 can be formedusing a splint, such as transventricular splint 12 shown in FIGS. 1 and2. Lobes 32 and 34 are joined at points 36 and 38. Points 36 and 38 areseparated by a distance l.

FIG. 5 is an idealized horizontal cross section of a left ventricle 40subdivided into three generally equal sized lobes 42, 44 and 46. Eachlobe has an equal radius and has an arc passing through an angle lessthan π. Adjacent ends of the lobes 48, 50 and 52 are separated by adistance l. A plurality of transventricular splints such as splint 12 asshown in FIGS. 1 and 2 could be extended between adjacent ends 48, 50and 52 to form lobes 42, 44 and 46.

For a restrictive splint, the horizontal cross sections 30 and 40 willhave a generally circular shape, i.e., a non-splinted shape at endsystole. As diastolic filling proceeds, the radius of the circular shapewill continue to increase until the splint engages. At the point thesplint engages, the lobed shape will begin to form. In the case of thetwo lobe splinting of FIG. 4, the radius will continue to increase asdiastolic filling proceeds. In the case of the three or more lobedshape, such as the three lobed configuration of FIG. 5, radius R willdecrease as diastolic filling proceeds. The radius will continue todecrease unless or until the pressure in the heart causes the heart toexpand such that the arc of the lobe passes through an angle θ greaterthan π.

In the case of a full cycle splint, at end systole, the splint willalready be engaged. Thus, for a full cycle splint at end systole, thehorizontal cross section of the chamber will not have the normalgenerally circular shape. Rather, at end systole, the horizontal crosssections 30 and 40 will have a lobed shape such as shown in FIGS. 4 and5. Subsequent shape change during diastolic filling for a full cyclesplint will be similar to that described with respect to restrictivesplints.

In view of LaPlace's Law which states that stress is directlyproportional to radius of curvature, it can be appreciated that whetherthe radius is increasing or decreasing during diastolic filling, willhave an impact on heart pumping performance. Where R is increasingduring diastolic filling, wall stress will increase more rapidly thanwhere R is decreasing. The number of lobes that are created cansignificantly influence the level of end diastolic muscle stressreduction achieved through splinting. Eventually adding additional lobesforms a configuration which approaches a behavior similar to a wrap. Ifa wrap is substantially inelastic, or of sufficient size, a wrap willonly engage the heart wall at some stage of diastolic filling. If thewrap is substantially inelastic, as pressure increases in the chamberduring diastolic filling, stress in the heart wall muscle will increaseuntil the wrap fully engages and substantially all additional muscleelongating load created by increased chamber pressure will be shifted tothe wrap. No further elongation of the chamber muscles disposed in ahorizontal cross section through the wrap and the chamber will occur.Thus, inelastic wraps will halt additional preload muscle strain (enddiastolic muscle stretch).

The type of shape change illustrated in FIGS. 4 and 5 is of substantialsignificance for restrictive splints. It is undesirable in the case ofrestrictive splints, to excessively limit preload muscle strain. TheFrank-Starling Curve demonstrates the dependence and need for variablepreload muscle strain on overall heart pumping performance. During aperson's normal activities, their body may need increased bloodperfusion, for example, during exertion. In response to increased bloodperfusion through a person's tissue, the heart will compensate for theadditional demand by increasing stroke volume and/or heart rate. Whenstroke volume is increased, the patient's normal preload strain is alsoincreased. That is, the lines 14-16 and 22-24 of the normal and failinghearts, respectively, will shift to the right. An inelastic wrap will,at engagement, substantially stop this shift. In the case of thebi-lobed shape change of FIG. 4 or a multiple lobed change having asmall number of lobes of FIG. 5, significant stress reduction can beachieved while allowing for variable preload strain. If the number oflobes is increased substantially, however, variable preload willdecrease as the multi-lobed configuration approaches the performance ofan inelastic wrap.

The magnitude of shape change in the case of full cycle splintingbecomes very important as full cycle splinting generally reduces chambervolume more than restrictive splinting. Although as with restrictivedevices, the type of shape change is also important to allow forvariable preload strain. Both restrictive device and full cycle splintsreduce chamber volume as they reduce the cross sectional area of thechamber during the cardiac cycle. The magnitude of the shape change canvary from very slight at end diastole, such that chamber volume is onlyslightly reduced from the unsplinted end diastolic volume, to an extremereduction in volume, for example, complete bifurcation bytransventricular splint. The magnitude of the shape change, for example,as measured by the ratio of splint length to non-splinted ventriculardiameter, is preferably modulated to reduce muscle stress while notoverly reducing chamber volume. For full cycle splint, the reduction ofchamber volume is compensated for by increased contractile shortening,which in turn leads to an increased ejection fraction, i.e., the ratioof the stroke volume to chamber volume. For given stress/volume andstress/shortening relationships, there will be a theoretical optimummaximal stroke volume. Clinically, 20% to 30% stress reduction isexpected to be attainable through full cycle bi-lobe splinting. See U.S.Pat. No. 5,961,440 and the discussion further herein for calculation ofstress reduction for idealized bi-lobe splinting.

When using the full cycle and restrictive devices described herein,caution should be exercised to limit the pressure on the coronaryvasculature. In the case of transventricular splints, valve structure,electrical pathways and coronary vasculature should be avoided.

FIG. 6 is a vertical view of a heart A similar to that shown in FIG. 1.Rather than having a single band splint surrounding heart A, there aretwo band splints 51 affixed to the heart by two transventricular splints52. Splints 52 include oppositely disposed anchors or anchor pads 53.FIG. 7 is a horizontal cross sectional view of heart A of FIG. 6, wraps51 and splint 52. Splints 52 include a tension member 54 disposedthrough left ventricle B. Pads 53 are disposed on the opposite ends oftension members 54. Right ventricle C is shown to the left of leftventricle B.

Splints 52 can be restrictive or full cycle splints. Band Splints 51 areshown as restrictive band splints as in FIG. 6, heart A is shown engagedwith the band splints 51, whereas in FIG. 7, heart A has contracted tomove away from band splints 51. Wraps 51 and splints 52 should be madefrom biocompatible materials. Band splints 51 are preferably made from apliable fabric or other material which resists elongation under normaloperating loads. Band splints 51 can, however, be made from an elasticmaterial which elongates during the cardiac cycle. Tension members 54also preferably resist elongation under normal operating loads. Tensionmembers 54 can, however, be made from an elastic material whichelongates during the cardiac cycle.

FIG. 8 is a vertical view of heart A, partial wrap 61 andtransventricular splint 62. Transventricular splint 62 includes anchorpads 63. FIG. 9 is a horizontal cross sectional view of heart A, partialband splint 61 and splint 62. Splint 62 is essentially similar to wrapor band splint 12 shown in FIGS. 1 and 2. Partial band splint 61 is alsoessentially similar to wrap or band splint 11 shown in FIGS. 1 and 2except that band splint 61 only surrounds a portion of heart A. Thisportion is shown in FIGS. 8 and 9 to the left including a portion ofleft ventricle B.

FIG. 10 is a horizontal cross sectional view of left ventricle B andright ventricle C of heart A taken at a similar elevation as that shownin FIG. 2. A splint 70 is shown disposed on heart A. Splint 70 includesa frame having two heart engaging anchors or pads 72 disposed at itsopposite ends. A third heart engaging pad 73 is disposed along frame 70approximately midway between pads 72.

Pads 72 are shown engaged with heart A to change the shape of ventricleB in FIG. 10. Pads 73 are not engaged with heart A in FIG. 10. FIG. 11is the same horizontal cross sectional view as FIG. 10 except that heartA has to contact pad 73 to create a further shape change of leftventricle B.

Frame 70 is preferably rigid enough that pads 72 could be disposed onthe heart for full cycle splinting and sufficiently adjustable that pads72 could be spaced further apart for restrictive splinting. Pad 73accomplishes restrictive splinting. Frame 71, pads 72 and 73 of splint70 are made of a biocompatible material. Pads 72 and 73 are preferablysubstantially atraumatic.

FIG. 12 is a vertical view of heart A shown in phantom line. Showndisposed about the ventricles of heart A is a basket-like band splint100. Band splint 100 includes a horizontal encircling band 101 around anupper region of the ventricles and four bands 102 which extend downwardtoward the apex of heart A. It can be appreciated that bands 102 can actas splints to form four lobes in heart A in a horizontal plane.Depending on the placement of bands 102 around heart A, lobes could becreated only in the left ventricle or in the left ventricle and/or otherchambers of the heart. Band 102 is joined at the apex. Band 101 and band102 can be made from a webbing, fabric or other biocompatible material.

If band splint 100 substantially elongated elastically under normaloperating loads, it could be friction fit to heart A and act full cycle,limiting muscle stress at end diastole as well end systole. Band splint100 could be sutured into place or otherwise held on heart A and act asa restrictive device. If band 101 were securely fastened to heart A,bands 102 could limit the vertical elongation of heart A duringdiastolic filling.

FIG. 13 is an alternate embodiment 110 of the band splint of FIG. 12.Band splint 110 includes a horizontally heart encircling band 111 andfour bands 113 extending downward from band 111. Bands 113, however,unlike bands 102 of band splint 100 do not extend to the apex of heartA, but rather to a second horizontally heart encircling band 112.

Band splint 110 could be made of the same materials as band splint 100.Band splint 110 can also be used in a manner similar to band splint 100except that band splint 110 would limit the vertical elongation of theventricles less than band splint 100.

FIG. 14 is yet another alternate embodiment 120 of the wrap of FIG. 12.Band splint 120 closely resembles alternate embodiment 110 of FIG. 13,except that rather than having four vertically extending web members,band splint 120 includes two substantially rigid members 123interconnecting two horizontally encircling web members 121 and 122.

FIG. 15 is yet another alternate embodiment 130 of the band splint ofFIG. 12. Like the wrap of FIG. 12, band splint 130 includes ahorizontally encircling member 131 and four downwardly extending members132. At a location proximate of the apex of heart A, members 132 arejoined by a ring 133. Members 132 extend through ring 133. Ring 133 canbe used to adjust the length of members 132 between band 131 and ring133. Ring 133 can be formed from metallic material and crimped inwardlyto fix its position along members 132. Other means of holding ring 133in position would be readily apparent to those skilled in the art.

FIG. 16 is a vertical view of heart A including a partial band splint140 secured around a substantial portion of left ventricle B. Bandsplint 140 includes a vertically elongating anchor member 141 whichsutures 142 can encircle to anchor member 141 to heart A. A band 143extends generally horizontally from anchor member 141 to an oppositeanchor 141.

The length of band 143 can be seen in its entirety in FIG. 17 which is ahorizontal cross sectional view of heart A through band 143, leftventricle B and right ventricle C. In FIG. 16, heart A is shown engagedwith band 143, however, in FIG. 17, band 143 is shown spaced from heartA. Thus, in this configuration, wrap 140 would be acting as arestrictive device. If band splint 140 were made from a material thatsubstantially deforms elastically under normal loads, band splint 140could also be secured sufficiently snuggly to heart A to act as a fullcycle device. Preferably, however, band 143 of band splint 140 is formedfrom a webbing or substantially inelastic fabric.

FIG. 18 is a vertical view of heart A including a wrap 160. Wrap 160 caninclude a single thread or line 161 encircling the heart several times.After line 161 encircles heart A, line 161 can be threaded through a bar162, including a plurality of eyelets 163 spaced along its length inpairs. Bar 162 is preferably rigid enough to substantially maintain thedistance between eyelets 163 under normal operating loads.

When line 161 is placed in heart A, one end of line 161 can be tied tobar 162 at 164. Line 161 can then encircle the heart and be drawnthrough eyelet 162 adjacent the beginning of line 161 at 164. Line 161can then be drawn through one eyelet 163 of a lower pair of eyelets toencircle the heart again. This process continues until line 161 is tiedto an eyelet 163 at 165. It can be appreciated that wrap 160 could beused as a restrictive or full cycle device depending on the diameter ofloop formed by line 161.

FIG. 19 is an alternate embodiment 170 of the wrap of FIG. 18. Wrap 170,however, includes two vertically extending bars 172 having eyelets 173through which line 171 is threaded. Line 171 can be tied to one of thebars 172 at 174 and 175.

FIG. 20 is a vertical view of heart A including yet another embodiment180 of the wrap of FIG. 18. Wrap 180 includes a line 181 encirclingheart A a plurality of times. Rather than having a single verticallyextending bar 162 to position line 180 on heart A, wrap 180 includes aplurality of horizontal bars 182 including a pair of eyelets 183. Oneend of line 181 is tied to an upper bar 182 at 184 and the opposite endof line 181 is tied to a lower bar 182 at 185. Between 184 and 185, line181 is threaded through eyelets 182 to form the heart encircling patternshown in FIG. 20.

FIG. 21 is a vertical view of heart A including yet another alternateembodiment 190 of the wrap of FIG. 18. Wrap 190 closely resembles 180 ofFIG. 20. Line 181 has, however, been threaded through eyelets 183 ofbars 182 in a pattern which, unlike that of FIG. 20, bars 182 aredisposed at various selected locations around the circumference of heartA.

FIG. 22 is a vertical view of heart A including a wrap 200. Wrap 200 issubstantially similar to wrap 11 of FIGS. 1 and 2, except that wrap 200extends vertically a greater distance than wrap 11. Wrap 200 is notshown with a transventricular splint. It can be appreciated that wrap200 could be used as restrictive or full cycle device.

FIG. 23 is a horizontal cross section of a human torso including heartA, left ventricle B, right ventricle C, lungs E and ribs G. A wrap 210is shown partially encircling heart A. Opposite ends of wrap 210 areanchored at 211 to ribs G. At 211, wrap 210 can be anchored to ribs G bybone screw, knot or other means of fastening. It can be appreciated thatband splint 210 could be used as a restrictive or full cycle device.

FIG. 25 is a vertical view of heart A having a horizontal width W₁. FIG.26 is an idealized horizontal cross sectional view of heart A of FIG.25. Heart A includes left ventricle B and right ventricle C. Leftventricle B has a radius R₁.

FIG. 27 is a view of a device 220. Device 220 includes a horizontallyencircling band 222 which can be affixed to heart A by sutures, otherattachment means or friction fit. Extending from band 222 is asubstantially rigid elongate member 224. Member 224 extends to the apexof heart A. Pin 226 extends into left ventricle B of the apex. An anchoror pad 228 is disposed within left ventricle B to anchor the apex ofheart A to elongate member 224. Elongate member 224 can be made ofsufficient length such that heart A is vertically elongate full cycle,or alternately not at end diastole.

FIG. 28 is a vertical view of an elongate heart A having a horizontalwidth W₂ less than W₁. FIG. 29 is a horizontal cross section of theheart A of FIG. 28 including left ventricle B and right ventricle C. InFIG. 29, the radius R₂ of left ventricle B is less than R₁ of FIG. 26.Assuming that the hearts of FIGS. 25 and 28 are at the same point in thecardiac cycle, it can be appreciated that the wall stress in heart A isless in FIG. 29 as R₂ is shorter R.

If elongate bar 224 is sized such that device 220 does not engage at enddiastole, but rather anchor pad 228 first engages during systoliccontraction, device 220 can fall into a third class of device neitherfull cycle nor restrictive. Such a device would reduce wall stressduring a portion of systolic contraction including end systole, but notreduce wall stress during end diastole, thus maintaining maximumpreload.

Band 222 of device 220 is preferably formed from a web material or otherfabric. Band 220 is preferably does not elongate substantially duringdiastolic filling. Members 224, 226 and 228 are formed from materialswhich remain substantially rigid under the influences of the forcesencountered during the cardiac cycle.

FIG. 30 is a horizontal cross sectional view of heart A including leftventricle B and right ventricle C. A device 260 including a thread orline 261 is disposed transventricularly and transmyocardially throughheart A. A portion of line 261 is disposed outside of heart A. Oppositeends of line 261 are connected at 262. Those portions of line 261outside heart A form loops 263. The size of loops 263 are exaggeratedfor purposes of illustration. It is assumed that heart A in the processof diastolic filling in FIG. 30, and loops 263 are sufficiently small,eventually heart A will engage loops 263. In such a configuration,device 260 is used as a restrictive device. Loops 263 could be sized,however, such that they engage full cycle.

Line 261 is preferably made from atraumatic biocompatible material. Thediameter of line 261 is preferably sufficiently great that cutting ofheart A does not occur during diastolic filling.

FIG. 31 is a horizontal cross sectional view of heart A including leftventricle B and right ventricle C and an alternate embodiment 270 of thedevice of FIG. 30. Device 270 includes a line 271 which does not extendtransventricularly but extends through the myocardium of heart A to formfour loops 273.

Device 270 can be formed from material similar to that used to formdevice 260. Additionally, device 270 can be made to function as arestrictive device or full cycle device in a manner similar to that ofdevice 260.

Line 261 and line 267 could be disposed within a tube to avoid cheesecutting of the myocardium. The tube may be highly flexible, yet durableenough to prevent the line from cheese cutting through the myocardium ofthe heart. Devices 260 and 270 could extend through the septum or rightventricle to avoid forming lobes in right ventricle C.

FIG. 32 is a vertical view of heart A including three devices 270disposed at three spaced elevations. An elongate generally rigid bar 274is disposed through loops 273 to distribute the load on heart A fromloops 273 across a larger area than lines 271 can alone.

It should be understood that although devices disclosed herein aredescribed in relation to the left ventricle of a human heart, thesedevices could also be used to reduce the radius or cross-sectional areaof the other chambers of a human heart in transverse or verticaldirections, or at an angle between the transverse and vertical.

FIG. 33 shows a transverse cross-section of a left ventricle 10′ and aright ventricle 12′ of a human heart 14′. FIG. 33 also shows anembodiment of the present invention deployed with respect to leftventricle 10′ of human heart 14′. Here a compression frame structure 300is engaged with heart 14′ at atraumatic anchor pads 310. A compressionmember 312 having an atraumatic surface 314 presses against a wall ofleft ventricle 10′ to reduce the radius or cross-sectional area thereof.

FIG. 34 is a transverse cross-sectional view of human heart 14′ showingyet another embodiment of the present invention. In this case a clamp400 having atraumatic anchor pads 410 biased toward each other is showndisposed on a wall of left ventricle 10′. Here the radius orcross-sectional area of left ventricle 10′ is reduced by clamping offthe portion of the wall between pads 410. Pads 410 can be biased towardeach other and/or can be held together by a locking device.

Each of the various embodiments of the present invention can be madefrom materials which can remain implanted in the human bodyindefinitely. Such biocompatible materials are well-known to thoseskilled in the art of clinical medical devices.

In use, the various embodiments of the present invention are placed inor adjacent the human heart to reduce the radius or cross-section areaof at least one chamber of the heart. This is done to reduce wall stressor tension in the heart or chamber wall to slow, stop or reverse failureof the heart.

To discuss further the stress reduction associated with splinting, FIG.35 is a view of a cylinder or idealized heart chamber 48′ which is usedto illustrate the reduction of wall stress in a heart chamber as aresult of deployment of the splint in accordance with the presentinvention. The model used herein and the calculations related to thismodel are, intended merely to illustrate the mechanism by which wallstress is reduced in the heart chamber. No effort is made herein toquantify the actual reduction which would be realized in any particularin vivo application.

FIG. 36 is a view of the idealized heart chamber 48′ of FIG. 35 whereinthe chamber has been splinted along its length L such that a “figureeight” cross-section has been formed along the length thereof. It shouldbe noted that the perimeter of the circular transverse cross-section ofthe chamber in FIG. 35 is equal to the perimeter of the figure eighttransverse cross-section of FIG. 36. For purposes of this model,opposite lobes of the figure in cross-section are assumed to be mirrorimages.

FIG. 37 shows various parameters of the figure eight cross-section ofthe splinted idealized heart chamber of FIG. 36. Where I is the lengthof the splint between opposite walls of the chamber, R₂ is the radius ofeach lobe, θ is the angle between the two radii of one lobe whichextends to opposite ends of the portion of the splint within chamber 48′and h is the height of the triangle formed by the two radii and theportion of the splint within the chamber 48′ (R₁ is the radius of thecylinder of FIG. 35). These various parameters are related as follows:h=R ₂ COS(θ/2)l=2R ₂ SIN(θ/2)R ₂ =R ₁π/(2π−θ)

From these relationships, the area of the figure eight cross-section canbe calculated by:A ₂=2π(R ₂)²(1−θ/2π)+hl

Where chamber 48′ is unsplinted as shown in FIG. 35, A₁, the originalcross-sectional area of the cylinder, is equal to A₂ where θ=180°, h=0and l=2R₂. Volume equals A₂ times length L and circumferential walltension equals pressure within the chamber times R₂ times the length Lof the chamber.

Thus, for example, with an original cylindrical radius of fourcentimeters and a pressure within the chamber of 140 mm of mercury, thewall tension T in the walls of the cylinder is 104.4 newtons. When a3.84 cm splint is placed as shown in FIGS. 36 and 37 such that I=3.84cm, the wall tension T is 77.33 newtons.

FIGS. 38 and 39 show a hypothetical distribution of wall tension T andpressure P for the figure eight cross-section. As θ goes from 180° to0°, tension T_(θ) in the splint goes from 0 to a 2T load where thechamber walls carry a T load.

Numerous characteristics and advantages of the invention covered by thisdocument have been set forth in the foregoing description. It will beunderstood, however, that this disclosure is, in many respects, onlyillustrative. Changes may be made in details, particularly in matters ofshape, size and ordering of steps without exceeding the scope of theinvention. The invention's scope is defined in the language of theclaims.

1. A method for reducing wall tension on at least one chamber of thenatural heart, comprising the steps of: providing a geometricreconfiguration assembly; encircling an external surface of the at leastone of the chambers of the natural heart in an unrestrained position,with said geometric reconfiguration assembly; and causing an inwarddisplacement of at least one portion of the natural heart and preventingthe natural heart from returning to the unrestrained position at enddiastole, with said geometric reconfiguration assembly, wherein thegeometric reconfiguration assembly includes a splint traversing the atleast one of the chambers of the natural heart.